Component

Cellular biotin uptake

Measured biotin accumulation in cellular transport assays.

8 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport.

    Carbamazepine → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"}
    experimental_model
    Transport assays in purified human intestinal brush-border and basolateral membrane vesicles
    exposure
    Carbamazepine or primidone; millimolar inhibitor constants
    limitations
    These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient.
    nutrient_topic
    Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
    organism
    Homo sapiens
    plain_language
    The drug competed with biotin at the gut-facing membrane in this experiment.
    primary_references
    [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
    tissue_or_cell_type
    Intestinal membrane vesicles
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 273–284

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport assays in purified human intestinal brush-border and basolateral membrane vesicles · source_derived_draft · unverified_draft

    ### b7-carbamazepine-uptake Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug competed with biotin at the gut-facing membrane in this experiment. organism: Homo sapiens tissue_or_cell_type: Intestinal membrane vesicles experimental_model: Transport assays in purified human intestinal brush-border and basolateral membrane vesicles limitations: These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient. exposure: Carbamazepine or primidone; millimolar inhibitor constants evidence_span: {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"} [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
    Complete structured claim and evidence

  2. Primidone competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 2.25 mmol/L), without inhibiting basolateral biotin transport.

    Primidone → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"}
    experimental_model
    Transport assays in purified human intestinal brush-border and basolateral membrane vesicles
    exposure
    Carbamazepine or primidone; millimolar inhibitor constants
    limitations
    These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient.
    nutrient_topic
    Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
    organism
    Homo sapiens
    plain_language
    The drug competed with biotin at the gut-facing membrane in this experiment.
    primary_references
    [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
    tissue_or_cell_type
    Intestinal membrane vesicles
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 286–297

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport assays in purified human intestinal brush-border and basolateral membrane vesicles · source_derived_draft · unverified_draft

    ### b7-primidone-uptake Primidone competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 2.25 mmol/L), without inhibiting basolateral biotin transport. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug competed with biotin at the gut-facing membrane in this experiment. organism: Homo sapiens tissue_or_cell_type: Intestinal membrane vesicles experimental_model: Transport assays in purified human intestinal brush-border and basolateral membrane vesicles limitations: These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient. exposure: Carbamazepine or primidone; millimolar inhibitor constants evidence_span: {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"} [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
    Complete structured claim and evidence

  3. Wild-type SLC19A3 did not confer detectable biotin uptake, whereas the SLC5A6 positive control did.

    Human thiamine transporter 2 / SLC19A3 → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Distinguishes thiamine transport from biotin transport; no shared-substrate mechanism demonstrated.
    evidence-scope
    Caco-2 and MDCK epithelial models
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}]
    experimental_model
    Human transporter constructs in epithelial cell lines; uptake and surface targeting.
    limitations
    Tested cell models; clinical biotin-response mechanism remains unresolved.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins in human and canine cell lines
    plain_language
    The name biotin-responsive disease does not make SLC19A3 a biotin carrier.
    primary_references
    [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
    tissue_or_cell_type
    Caco-2 and MDCK epithelial models

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 294–307

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in epithelial cell lines; uptake and surface targeting. · source_derived_draft · unverified_draft

    ### b1-slc19a3-not-biotin-transporter Wild-type SLC19A3 did not confer detectable biotin uptake, whereas the SLC5A6 positive control did. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The name biotin-responsive disease does not make SLC19A3 a biotin carrier. organism: Human proteins in human and canine cell lines tissue_or_cell_type: Caco-2 and MDCK epithelial models experimental_model: Human transporter constructs in epithelial cell lines; uptake and surface targeting. limitations: Tested cell models; clinical biotin-response mechanism remains unresolved. cross_nutrient: Distinguishes thiamine transport from biotin transport; no shared-substrate mechanism demonstrated. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}] evidence_locator: Abstract evidence-scope: Caco-2 and MDCK epithelial models [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
    Complete structured claim and evidence

  4. Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay.

    Lipoic acid → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
    exposure
    Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.
    limitations
    In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay.
    primary_references
    [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
    tissue_or_cell_type
    HEK293T cells expressing human SMVT

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 444–455

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft

    ### b5-trans-lipoate-inhibits-biotin Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
    Complete structured claim and evidence

  5. D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay.

    Pantothenate (vitamin B5) → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
    exposure
    Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.
    limitations
    In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    D-pantothenic acid competed with biotin uptake in the SMVT cell assay.
    primary_references
    [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
    tissue_or_cell_type
    HEK293T cells expressing human SMVT

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 431–442

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft

    ### b5-trans-pantothenate-inhibits-biotin D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: D-pantothenic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
    Complete structured claim and evidence

  6. Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.

    Human SLC5A6 R123L protein variant → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
    exposure
    Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.
    limitations
    Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    The R123L SMVT variant lost the uptake activity seen with the normal transporter.
    primary_references
    [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
    tissue_or_cell_type
    HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 353–364

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft

    ### b5-trans-r123l-biotin Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R123L SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
    Complete structured claim and evidence

  7. Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.

    Human SLC5A6 R94X truncated protein → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
    exposure
    Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.
    limitations
    Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    The R94X SMVT variant lost the uptake activity seen with the normal transporter.
    primary_references
    [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
    tissue_or_cell_type
    HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 340–351

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft

    ### b5-trans-r94x-biotin Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R94X SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
    Complete structured claim and evidence

  8. Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin.

    Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
    exposure
    Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
    limitations
    Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens (protein and HRPE expression cells)
    plain_language
    SMVT carries biotin into cells using sodium-dependent transport.
    primary_references
    [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
    tissue_or_cell_type
    HRPE cell plasma membrane

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 171–182

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft

    ### b5-trans-smvt-biotin Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries biotin into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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